Updated: Aug 30, 2019
Since my previous articles on medical emergencies, I have been getting a lot of requests to write about anaphylaxis.
But I wanted to write about some lighter topics after the heavy topics like Adrenal insufficiency and Ischemic heart diseases. That is why I wrote about Radiology of Maxillary sinus in the previous post.
As I mentioned in my earlier posts, I will be dividing this topic into two articles.
In the first article, I will be talking about pathophysiology of anaphylaxis and in the next one I will talk about management and prevention of anaphylaxis.
I apologize for the lack of images in this article. I wrote this article on my mobile phone using mobile data. I do not have access to a computer as I am stranded in another city because of heavy rains.
I will update the pics when I am back at my place.
So now that I am done with all the cliche stuff, let's get started.
I'll first talk a bit about allergy in general.
Allergy is just a hypersensitive reaction of our immune system to a usually harmless substance. This harmless substance can be bee sting, pollen, milk, strawberry, latex, local anesthesia etc.
Basically, there are 4 types of allergies based on the mechanism (by Coombs and Gell).
They are :
Type 1 - Anaphylaxis
Type 2 - Antibody-mediated cytotoxic reactions
Type 3 - Immune complex-mediated reactions
Type 4 - Delayed type hypersensitivity
Of those, Type 1 (IgE mediated, Immediate response, Life threatening) and Type 4 (Cell mediated, delayed response) are of concern to a general dentist.
Type 1 is anaphylaxis whereas example of Type 4 allergy is contact dermatitis or itching because of latex or other dental material in dentists or patients.
Let us talk about the pathophysiology of Anaphylaxis in a chronological order.
When a person is first exposed to an Allergen (like pollen, Local Anesthesia, Bee sting), there is production of IgE Antibodies in a large amount from plasma cells. These IgE antibodies go and attaches to the mast cells.
When the person is exposed to the same allergen second time, these Mast cells release chemical mediators like Histamines and Cytokines.
Depending on the site on which these chemical mediators act, we get different signs and symptoms of allergy.
A person never shows the signs of allergy at the first exposure to allergen. The signs are observed after the first exposure depending on the speed at which antibodies against those allergens are produced in the body.
These chemical mediators can act on nerve fibres, mucous membrane and blood vessels.
Their action on nerve fibres lead to pain, itching and smooth muscles contractions.
Smooth muscles are found in lungs (bronchi) and in Gastro-Intestinal Tract (GIT). So smooth muscles contractions lead to bronchospasm and severe abdominal cramps.
These abdominal cramps will force the content of GIT upwards to the oral cavity (causing Vomiting) or downwards to the rectum (causing Diarrhea).
The action of chemical mediators on mucous membrane is increased mucus secretion leading to partial blockage of the bronchi. This along with bronchospasm leads to a major blockage of the bronchi (although partial). There is still some amount of air exchange in the lungs.
This appears clinically as wheezing sound made by the patient while breathing.
The action of these chemical mediators on blood vessels is increased permeability and vasodilation. Vasodilation leads to pooling of blood under skin and peripheries causing erythema (reddish color of skin).
Increased permeability causes increase in interstitial tissue fluid leading to swelling in various parts.
This causes increased tissue fluid in the nasal mucosa, leading to vasomotor rhinitis (running nose) and swelling in different parts of body (Angioedema).
Because of this edema, you may also see Hives on skin. These are always accompanied by intense itching.
Increased permeability also shows clinically as Laryngeal Edema which is a life-threatening condition. Here there is complete blockage of the upper airway because of the swelling of vocal cords.
When there is laryngeal edema, there is zero exchange of gases. Hence patient is not able to breathe, this is called as Dyspnea.
The two conditions (Bronchospasm & Laryngeal edema) lead to hypoxia (reduced oxygen concentration) which shows as cyanosis (bluish discoloration) of skin, mucous membrane and Nails.
To counter the reduced oxygen levels in different organs of the body, heart starts beating at a faster rate. This is Tachycardia.
But as myocardium itself is in hypoxic state, this leads to less force of contraction. Also, there is peripheral pooling of blood due to generalized vasodilation leading to reduced venous return. These two things lead to Hypotension.
If myocardium is in this hypoxic state for a long duration then it will lead to IHD leading to chest pain and then tissue death in myocardium causing dysrhythmia. (Read about this in detail here)
This will cause reduced blood supply to brain, causing unconsciousness. (Read about this in detail here)
If this generalized hypoxic state is continued for a longer duration then it will lead to cardiac arrest and then death of the patient.
So let us list the signs that you'll see in anaphylaxis.
Nausea & vomiting
Erythema (flushing of skin)
Chest pain (ihd)
Remember, the above explained cascade occurs in the matter of minutes. The above mentioned signs are seen in combination, not one after the other.
You have a very small window of opportunity to accurately diagnose and then manage Anaphylaxis.
So now you know what signs you are supposed to look for to diagnose Anaphylaxis.
A delay in diagnosis can cost you the life of your patient, especially in case of Anaphylaxis.
Let me know in the comment section, have any of your patient had any allergic reaction and how did you manage it.
Also, do let me know what topics would you want me to write about in future. If you find my posts helpful then share it on Whatsapp, Facebook or Twitter or any other social media platform that you use.